Discriminating between mothers' infant- and adult-directed speech: Cross-linguistic generalizability from Japanese to Italian and German.

The aim of the present work was a cross-linguistic generalization of Inoue et al.'s (2011) algorithm for discriminating infant- (IDS) vs. adult-directed speech (ADS). IDS is the way in which mothers communicate with infants; it is a universal communicative property, with some cross-linguistic differences. Inoue et al. (2011) implemented a machine algorithm that, by using a mel-frequency cepstral coefficient and a hidden Markov model, discriminated IDS from ADS in Japanese. We applied the original algorithm to two other languages that are very different from Japanese - Italian and German - and then tested the algorithm on Italian and German databases of IDS and ADS. Our results showed that: First, in accord with the extant literature, IDS is realized in a similar way across languages; second, the algorithm performed well in both languages and close to that reported for Japanese. The implications for the algorithm are discussed.

Work satisfaction of Japanese public health nurses: assessing validity and reliability of a scale.

The Index of Work Satisfaction, developed by Stamps et al., was administered to 583 nurses who had practiced public health nursing in Japan. After psychometric evaluation, three components were identified as contributing to their job satisfaction: the work environment, professional confidence, and commitment to the profession. Overall, the participants in the study were quite satisfied. The findings corroborated previous reports on Japanese nurses' job satisfaction, in that the nurses in the study were most satisfied with their relationships with peers, patients/families, and supervisors. However, they were least satisfied with having enough time for client care, having confidence, and promotion opportunities. The implications are discussed, to the effect that understanding the factors related to public health nurses' job satisfaction could help administrators to improve regulations and other issues related to the work environment.

Redesign of a static horizontal elutriator to perform according to the ISO 7708 respirable convention.

A static horizontal elutriator (multi-channel elutriator C-30, Sibata Scientific Instruments Ltd, Tokyo) has been widely used as a dust size classifier for a low-volume air sampler in Japan. The sampler uses the historical criterion defined by the British Medical Research Council (BMRC). However, a new sampling convention based on the ISO 7708 respirable dust convention was recently introduced into the Japanese standard for work environment measurement. It is necessary to modify the multi-channel static horizontal elutriator to satisfy the ISO 7708 respirable convention. We propose a modification of the horizontal elutriator, involving the shortening of 11 of the 36 plates to meet the ISO 7708 respirable convention. The relationship between aerosol particle size and penetration for the elutriator was measured in calm air. The measured penetrations were compared with the calculated performance of the sampler and with the sampling convention for the ISO respirable dust. The calculated bias of sampled masses with respect to the ISO respirable mass was almost zero for the workplace aerosols.

Calcitonin gene-related peptide (CGRP) as hazard marker for lung injury induced by dusts.

Calcitonin gene-related peptide (CGRP), which has a function as a growth factor of epithelial cells, is thought to play a role in pulmonary epithelium repair. In order to establish whether or not CGRP is associated with repair in lung damaged by dust, we examined gene expression of CGRP in the lungs of animal models exposed to different dusts. Male Wistar rats were administered 2 mg of crystalline silica, crocidolite, potassium octatitanate whisker (PT-1), and silicon carbide whisker (SiCW) suspended in saline by a single intratracheal instillation and were sacrificed at 3 d, 1 wk, 1 mo, 3 mo, and 6 mo of recovery time. Pathological findings of advanced pulmonary fibrosis were present in the rats exposed to crystalline silica and crocidolite through the experiment, whereas findings of mild or reversible pulmonary fibrosis were present in those exposed to SiCW and PT-1. The expression of CGRP in rat lung was observed by reverse-transcription polymerase chain reaction (RT-PCR) and enzyme immunometric assay (EIA). In RT-PCR, CGRP gene expression was decreased at the interval of 3 d and 1 wk in the case of crystalline silica and crocidolite; on the other hand, it was increased at 3 d and 1 wk in SiCW and at 3 d, 1 wk, and 3 mo in PT-1-exposed rats. CGRP protein level in lungs exposed to PT-1 and SiCW was also higher than that to silica and crocidolite at 3 d of recovery time. These data suggest that CGRP is associated with repair in lung damaged by different dusts, and that CGRP could be used as a sensitive biomarker to indicate the pathogenicity of dusts.

Change of heme oxygenase-1 expression in lung injury induced by chrysotile asbestos in vivo and in vitro.

Oxidative stress is thought to be the pathogenesis of pulmonary fibrosis induced by asbestos, and heme oxygenase-1 (HO-1) protects lung tissue against oxidative stress. We hypothesized that HO-1 is also associated with oxidative lung injury caused by exposure to chrysotile asbestos. This study was conducted to investigate the HO-1 expression of lungs in lung injury by chrysotile asbestos in vivo and in vitro. Male Wistar rats were administered 1 mg or 2 mg chrysotile suspended in saline by a single intratracheal instillation and were sacrificed at 3 days, 1 wk, 1 mo, 3 mo, and 6 mo of recovery time. The expression of HO-1 was observed by Western blot analysis, reverse-transcription polymerase chain reaction, and immunostaining. Protein levels of HO-1 increased at from 3 days to 6 mo following intratracheal instillation of 1 or 2 mg chrysotile. The mRNA levels of HO-1 increased at 3 mo and 6 mo following intratracheal instillation of 1 or 2 mg chrysotile. HO-1-positive cells were mainly found in the alveolar macrophages during immunostaining. We then examined HO-1 protein expression in human alveolar epithelial cells (A549). A549 cells were incubated with chrysotile at concentrations of 0, 12.5, 25, 50, and 100 microg/ml over 24 h. Increased expression of HO-1 protein was found following exposure to 25 or 50 microg/ml of chrysotile. Increased expression of HO-1 was also found at 6, 12, 24, and 48 h after exposure to 50 microg/ml of chrysotile with a peak at 24 h. These findings suggest that HO-1 is related to lung injury arising from exposure to chrysotile asbestos in vivo and in vitro.

Expression of heme oxygenase-1 in the lungs of rats exposed to crystalline silica.

Oxidative stress is thought to be the pathogenesis of pulmonary fibrosis induced by particles, and heme oxygenase-1 (HO-1) protects lung tissue against oxidative stress. We hypothesized that HO-1 is also associated with oxidative lung injury caused by exposure to particles. The present study was conducted to investigate the time course of HO-1 expression of lungs exposed to crystalline silica in vivo. Male Wistar rats were administered 1 mg or 2 mg of crystalline silica suspended in saline by a single intratracheal instillation and were sacrificed at 3 d, 1 wk, 1 month, 3 months and 6 months of recovery time. The expression of HO-1 was observed by western blot analysis and immunostaining. Protein levels of HO-1 were increased compared to the controls at 3 d, and from 1 month to 6 months following intratracheal instillation of 2 mg of crystalline silica. The levels of HO-1 were increased compared to the controls from 1 month to 6 months following intratracheal instillation of 1 mg of crystalline silica. Many HO-1 positive cells were found particularly in the alveolar macrophages during immunostaining. These findings suggest that HO-1 is related to lung injury arising from exposure to crystalline silica.

Phospholipid concentration in lung lavage fluid as biomarker for pulmonary fibrosis.

Pulmonary surfactant comprised primarily of phospholipids is a phospholipid-protein complex synthesized by type II alveolar epithelial cells or Clara cells and secreted to the pulmonary alveoli. As changes have been found in phospholipid concentrations in the bronchoalveolar lavage fluid (BALF) of patients with pulmonary fibrosis, phospholipid is considered to be involved in the process of fibrois/fibrotic process. Therefore, we made a crystalline silica rat model and measured phospholipid concentrations in lung lavage fluid in order to study the relationship of phospholipid to particle-induced pulmonary fibrosis. Eight-week-old Wistar male rats (n = 35) were injected with 2 mg crystalline silica particles suspended in 0.4 ml physiological saline. Rats in the control group (n = 35) were injected with physiological saline only. There were 7 rats in each of the ten subgroups. Rats were sacrificed and dissected at 3 days, 1 wk, 1 mo, 3 mo, and 6 mo after injection. Bronchoalveolar lavage was conducted on bronchoalveoli recovered from the right lung of each rat, the lavage fluid was centrifuged, and the supernatant was used to measure phospholipid concentration. The results were compared with previously reported inflammation scores. Phospholipid concentrations in lung lavage fluid for the exposed group showed a statistically significant increase compared to the control group throughout the observation period. Moreover, when compared to histopathologically examined inflammation scores, a positive correlation was found between the two. Judging from the facts that phospholipid concentrations in lung lavage fluid increased and that this increase correlated with the severity of inflammation, this experiment indicated that phospholipids are involved in particle-induced lung disorders.

Expression of clara cell secretory protein in the lungs of rats exposed to crystalline silica in vivo.

It has been theorized that Clara cell secretion protein (CCSP) plays a critical role in regulating the acute inflammatory response in the lung. We hypothesized that CCSP is also related to lung injury induced by occupational dust. The present study was conducted to investigate the time course of the expression of CCSP in lungs exposed to crystalline silica in vivo. Male Wistar rats were administered 1 mg or 2 mg of silica suspended in saline by a single intratracheal instillation and were sacrificed at 3 d, 1 wk, 1 month, 3 months and 6 months of recovery time. The expression of CCSP was observed by RT-PCR and western blot analysis. Exposure to 2 mg of silica decreased in levels of CCSP mRNA at 3 d, 1 wk, 1 month and 6 months following intratracheal instillation. The protein level of CCSP in silica-exposed rats was decreased at 3 d, 7 d and 1 month after a single instillation of 2 mg. The decreases in CCSP at the acute phase in this experiment suggest that CCSP may regulate the acute injury of the lung exposed to silica.

Expression of heme oxygenase-1 in the lungs of rats exposed to crocidolite asbestos.

Oxidative stress is thought to be the pathogenesis of pulmonary fibrosis induced by asbestos, and heme oxygenase-1 (HO-1) protects lung tissue against oxidative stress. We hypothesized that HO-1 is associated with oxidative lung injury caused by exposure to asbestos. This study was conducted to investigate the time course of HO-1 expression of lungs exposed to crocidolite asbestos in vivo. Male Wistar rats were administered 1 mg or 2 mg crocidolite asbestos suspended in saline by a single intratracheal instillation and were sacrificed at 3 d, 1 wk, 1 mo, 3 mo, and 6 mo of recovery time. The expression of HO-1 was observed by Western blot analysis and immunostaining. Protein levels of HO-1 increased at from 3 d to 6 mo following intratracheal instillation of 2 mg crocidolite asbestos. The levels of HO-1 increased at 1 wk and 1 mo following intratracheal instillation of 1 mg crocidolite asbestos. Many HO-1-positive cells were found, particularly in the alveolar macrophages, during immunostaining. These findings suggest that HO-1 may be related to lung disorder induced by dust and therefore can act as a biomarker of lung injury due to dust exposure.

[Method for installing an effective smoking room and the effectiveness of real-time monitoring].

We investigated the methodology for installing effective smoking rooms in workplaces. It is absolutely necessary to install exhaust ventilation in smoking rooms. There are two bases for deciding the exhaust ventilation rate. The most important is to eliminate the leakage of environmental tobacco smoke (ETS) from the smoking room. An airflow rate of more than 0.2 m/s at the opening of the smoking room is required by the Guidelines for Smoking Control in Workplaces (Ministry of Labour, Welfare and Health) to eliminate the leakage. This ventilation rate is decided by multiplying the opening area by 0.2 m/s. The second important point is to keep the concentration of ETS in the smoking room less than control concentration (0.15 mg/m3). This ventilation rate is decided by dividing the rate of generation of ETS by the control concentration. It is confirmed that an effective smoking room can be installed by following these guidelines. We used real-time monitoring to evaluate the leakage of ETS from the smoking room and the ETS concentration in the smoking room before and after the improvement. It is concluded that real-time monitoring of ETS is a useful method for evaluating the effectiveness of the smoking room.